IL-6 Signaling Link between Inflammatory Tumor Microenvironment and Prostatic Tumorigenesis

Benign prostatic hyperplasia and prostate cancer are tumoral pathologies characterized by the overexpression of inflammatory processes. The exploration of tumor microenvironment and understanding the sequential events that take place in the stromal area of the prostate could help for an early manage...

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Main Authors: Cosmin-Victor Ene, Ilinca Nicolae, Bogdan Geavlete, Petrisor Geavlete, Corina Daniela Ene
Format: Article
Language:English
Published: Wiley 2022-01-01
Series:Analytical Cellular Pathology
Online Access:http://dx.doi.org/10.1155/2022/5980387
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author Cosmin-Victor Ene
Ilinca Nicolae
Bogdan Geavlete
Petrisor Geavlete
Corina Daniela Ene
author_facet Cosmin-Victor Ene
Ilinca Nicolae
Bogdan Geavlete
Petrisor Geavlete
Corina Daniela Ene
author_sort Cosmin-Victor Ene
collection DOAJ
description Benign prostatic hyperplasia and prostate cancer are tumoral pathologies characterized by the overexpression of inflammatory processes. The exploration of tumor microenvironment and understanding the sequential events that take place in the stromal area of the prostate could help for an early management of these pathologies. This way, it is feasible the hypothesis that normalizing the stromal environment would help to suppress or even to reverse tumor fenotype. A number of immunological and genetic factors, endocrine dysfunctions, metabolic disorders, infectious foci, nutritional deficiencies, and chemical irritants could be involved in prostate tumor development by maintaining inflammation, affecting local microcirculation, and promoting oxidative stress. Inflammatory processes activate hyperproliferative programs that ensure fibromuscular growth of the prostate and a number of extracellular changes. Acute and chronic inflammations cause accumulation of immunocompetent cells in affected prostate tissue (T cells, macrophages, mastocytes, dendritic cells, neutrophils, eosinophils, monocytes). Prostate epithelial and stromal cells, peri-prostatic fat cells, prostatic microvascular endothelial cells, and inflammatory cells produce cytokines, generating a local inflammatory environment. Interleukin-6 (IL-6) proved to be involved in the prostate tumor pathogenesis. IL-6 ability to induce pro- and anti-inflammatory responses by three mechanisms of signal transduction (classical signaling, transsignaling, cluster signaling), to interact with a diversity of target cells, to induce endocrine effects in an autocrine/paracrine manner, and the identification of an IL-6 endogenous antagonist that blocks the transmission of IL-6 mediated intracellular signals could justify current theories on the protective effects of this cytokine or by alleviating inflammatory reactions or by exacerbating tissue damage. This analysis presents recent data about the role of the inflammatory process as a determining factor in the development of benign and malign prostate tumors. The presented findings could bring improvements in the field of physiopathology, diagnosis, and treatment in patients with prostate tumors. Modulation of the expression and activity of interleukin-6 could be a mean of preventing or improving these pathologies.
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spelling doaj-art-44cc8a861de14f3f8329dc7bb3e4adf52025-08-20T02:37:48ZengWileyAnalytical Cellular Pathology2210-71852022-01-01202210.1155/2022/5980387IL-6 Signaling Link between Inflammatory Tumor Microenvironment and Prostatic TumorigenesisCosmin-Victor Ene0Ilinca Nicolae1Bogdan Geavlete2Petrisor Geavlete3Corina Daniela Ene4“Carol Davila” University of Medicine and Pharmacy“Victor Babes” Clinical Hospital of Infectious and Tropical Diseases“Carol Davila” University of Medicine and Pharmacy“Carol Davila” University of Medicine and Pharmacy“Carol Davila” University of Medicine and PharmacyBenign prostatic hyperplasia and prostate cancer are tumoral pathologies characterized by the overexpression of inflammatory processes. The exploration of tumor microenvironment and understanding the sequential events that take place in the stromal area of the prostate could help for an early management of these pathologies. This way, it is feasible the hypothesis that normalizing the stromal environment would help to suppress or even to reverse tumor fenotype. A number of immunological and genetic factors, endocrine dysfunctions, metabolic disorders, infectious foci, nutritional deficiencies, and chemical irritants could be involved in prostate tumor development by maintaining inflammation, affecting local microcirculation, and promoting oxidative stress. Inflammatory processes activate hyperproliferative programs that ensure fibromuscular growth of the prostate and a number of extracellular changes. Acute and chronic inflammations cause accumulation of immunocompetent cells in affected prostate tissue (T cells, macrophages, mastocytes, dendritic cells, neutrophils, eosinophils, monocytes). Prostate epithelial and stromal cells, peri-prostatic fat cells, prostatic microvascular endothelial cells, and inflammatory cells produce cytokines, generating a local inflammatory environment. Interleukin-6 (IL-6) proved to be involved in the prostate tumor pathogenesis. IL-6 ability to induce pro- and anti-inflammatory responses by three mechanisms of signal transduction (classical signaling, transsignaling, cluster signaling), to interact with a diversity of target cells, to induce endocrine effects in an autocrine/paracrine manner, and the identification of an IL-6 endogenous antagonist that blocks the transmission of IL-6 mediated intracellular signals could justify current theories on the protective effects of this cytokine or by alleviating inflammatory reactions or by exacerbating tissue damage. This analysis presents recent data about the role of the inflammatory process as a determining factor in the development of benign and malign prostate tumors. The presented findings could bring improvements in the field of physiopathology, diagnosis, and treatment in patients with prostate tumors. Modulation of the expression and activity of interleukin-6 could be a mean of preventing or improving these pathologies.http://dx.doi.org/10.1155/2022/5980387
spellingShingle Cosmin-Victor Ene
Ilinca Nicolae
Bogdan Geavlete
Petrisor Geavlete
Corina Daniela Ene
IL-6 Signaling Link between Inflammatory Tumor Microenvironment and Prostatic Tumorigenesis
Analytical Cellular Pathology
title IL-6 Signaling Link between Inflammatory Tumor Microenvironment and Prostatic Tumorigenesis
title_full IL-6 Signaling Link between Inflammatory Tumor Microenvironment and Prostatic Tumorigenesis
title_fullStr IL-6 Signaling Link between Inflammatory Tumor Microenvironment and Prostatic Tumorigenesis
title_full_unstemmed IL-6 Signaling Link between Inflammatory Tumor Microenvironment and Prostatic Tumorigenesis
title_short IL-6 Signaling Link between Inflammatory Tumor Microenvironment and Prostatic Tumorigenesis
title_sort il 6 signaling link between inflammatory tumor microenvironment and prostatic tumorigenesis
url http://dx.doi.org/10.1155/2022/5980387
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